To link to the entire object, paste this link in email, IM or documentTo embed the entire object, paste this HTML in websiteTo link to this page, paste this link in email, IM or documentTo embed this page, paste this HTML in website

Brain injury research utilizes animal models to examine the neuronal and neurological effects of damage, including reparative or compensatory cellular and molecular responses to injury. The experiments outlined in this thesis use an established model of motor cortex injury in rats to examine the mechanisms involved in determining the response to damage, with the goal of identifying endogenous factors or pathways that can be therapeutically manipulated to promote neural and behavioral functional recovery.; Following aspiration of the forelimb representation area of rat motor cortex, reactive changes are observed in growth-associated proteins, neuron and synapse morphology, and behavioral performance. Upregulation of the growth-associated proteins GAP-43 and SCG10 may underlie structural adaptations, such as multiple synaptic bouton formation, that compensate for weakened signals. Behaviorally, animals demonstrate deficits in sensorimotor ability and fine skilled usage of the forelimbs.; In these studies, we found that rats from different strains exhibit different behavioral profiles normally, and produce different growth-associated protein and neural remodeling responses to lesion. Their post-lesion behavioral recovery, however, is comparable. Strain considerations may be useful in designing studies that focus on these phenomena, and are critical to valid interpretation and generalization of study findings.; The studies documented here also show that both behavioral outcome and protein induction in response to cortical aspiration are dependent on intact nigrostriatal input. More specifically, striatal dopamine D1-type receptor function supports growth-associated protein induction, as well as spontaneous behavioral improvement. Finally, daily practice in a skilled reaching task can improve forepaw performance after lesioning, and the ability to develop a successful grasping strategy also involves striatal D1 receptors. In the rat cortical lesion model, intact striatal dopamine function appears to support endogenously activated mechanisms of recovery or compensation, highlighting the possibility of therapeutically manipulating the dopamine pathway to promote functional recovery.